Maternal and infant serum carotenoids are associated with infantile atopic dermatitis development
Authors: Yuzaburo Inoue, Yu Yamamoto, Shigenori Suzuki, Shingo Ochiai, Akifumi Eguchi, Taiji Nakano, Fumiya Yamaide, Satomi Hasegawa, Hiroyuki Kojima, Chisato Mori, Yoichi Kohno, Hiroyuki Suganuma, Naoki Shimojo
Journal: Allergy (2023)

Epidemiological studies have shown that eczema/atopic dermatitis (AD) in infancy is a risk for skin sensitization to allergens1 and allergic diseases development later in life.2 In mammals,3 carotenoids must be supplied via dietary intake of vegetables, fruits, or certain animal products. Carotenoids prevent allergic reactions via their provitamin A activity and high antioxidant potential. However, previous studies evaluating the association between maternal vegetable intake during pregnancy and eczema in offspring have shown inconsistent results.4-6 These studies did not measure the individual serum carotenoid levels of mothers or children and in breast milk; therefore, appropriate nutritional interventions in maternal and early infant intake of foods containing carotenoids to prevent AD remain unclear. In this study, we measured the total carotenoid levels and some of their sub-types in the mothers' serum at 36 weeks of gestation and children and in maternal breast milk to evaluate the association between carotenoid levels and the presence of doctor-diagnosed AD in 1-year-old infants. We compared participants' characteristics and exposures by 1 year of age (Table S1); carotenoid, retinol, and α-tocopherol levels (Table 1) in the participants' serum, with and without AD at 1 year of age, were compared to those in the serum and breast milk of their respective mothers. We found that both the presence of eczema by 6 months of age (evaluated by questionnaire) (odds ratio [OR], 31.7; 95% confidence interval [CI] 13.2–76.0) and S. aureus carriage in the skin by 6 months of age (OR, 5.20; 95% CI [2.30–11.75]) were associated with higher odds of AD development at 1 year of age. Whereas certain carotenoid levels and total carotenoid levels in the serum and breast milk were associated with lower odds of AD at 1 year. To avoid multicollinearity in the regression analysis, we selected seven relevant predictive variables among the carotenoid data using variable importance in projection scores in the partial least squares (PLS) analysis (Table S2). Stepwise logistic regression analysis using explanatory baseline characteristics, exposure by 1 year of age, and the seven selected carotenoid levels revealed that the following variables were significantly related to AD at 1 year of age (Table 2): presence of eczema by 6 months of age (OR, 34.5; p < .0001), maternal blood lutein level (OR, 0.002; p = .002), and infant blood lycopene level at 1 year (OR, 0.01; p = .007). We saw no association with any of the breastmilk levels studied. One strength of this study is that multiple biological sample types were used as proxies for carotenoid intake. The maternal blood's lutein concentration at 36 weeks of gestation, associated with a reduced AD risk at 1 year of age in the multivariate analysis, was significantly correlated with the cord blood lutein level (Table S3). This suggests that lutein ingested during pregnancy is transferred to the fetus and may inhibit AD development in infancy. Another strength of this study is that simultaneous evaluation of the concentrations of lutein, zeaxanthin, α-carotene, β-carotene, and lycopene showed a strong correlation, suggesting biasness in the preference for foods containing these carotenoids (e.g., vegetables and fruits) (Table S4). Although the carotenoid intake mechanism that prevents AD development remains unclear, the protective effect of lycopene and lutein on AD might be due to their ability to scavenge free radicals, reduce oxidative stress, and regulate the immune system. In conclusion, children of mothers with low carotenoid intake during pregnancy are at higher risk for developing infantile AD and are ideal targets for early intervention in allergy prevention. Further studies are needed to clarify whether carotenoid supplementation during pregnancy/lactation and infants after weaning may reduce AD development in infancy. We thank the children and families involved in the CHIBA study for all their support. We also thank Dr Hiroko Suzuki and Yuka Kobayashi for supporting the study. The research was funded by AMED-Innovative Advanced Research and Development Support (AMED-CREST) grant J17JK00058 and was conducted with funds provided by RIKEN based on the Joint Research Agreement between Chiba University and RIKEN. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Appendix S1: Figure S1: Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.